| Project/Area Number |
11671379
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Cerebral neurosurgery
|
|---|
| Research Institution | Nara Medical University |
|---|
Principal Investigator |
NAKASE Hiroyuki Nara Medical University, Assistant Professor, 医学部, 講師 (10217739)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
URANISHI Ryunosuke Nara Medical University, Research Associate, 医学部, 助手 (80245084)
|
|---|
| Project Period (FY) |
1999 – 2001
|
| Project Status |
Completed (Fiscal Year 2001)
|
| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 2001: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2000: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1999: ¥1,400,000 (Direct Cost: ¥1,400,000)
|
|---|
| Keywords | Penumbra / Cerebral blood flow / 脳虚血 / 薬剤性虚血耐性現象 / 脳血流脳酸素代謝 |
|---|
| Research Abstract |
The purpose of the present study was to make a penumbra-like condition model by the combination of CSD under hypobaric hypertension state in the rats. Twenty-four male Wister rats were used Local CBF, DC potential, brain tissue impedance were measured continuously for 45 minutes after hypertension beginning. CSD was induced once with potassium chloride (KC1) at fifth minutes after hypertension beginning in nine rats (group A) and under norm tension state in seven rats (group B). Eight rats (group C) had only hypertension state without KC1-induced CSD. DC potential, tissue impedance, 1CBF, neuronal damage, and postoperative body weight changes were compared among each group. Histology was studied at seventh day after operation. Local CBF did not increase by CSD, DC potential needed the time to normalize, and tissue impedance lasted in the state of a high value after KC1 injection during hypertension in group A (P < 0.05). Local CBF, DC potential, tissue impedance increase transiently after KC1 injection in group B and there were no significant change in the parameter except that 1CBF was dropped by hypertension in group C. Neuronal damage was observed severer in group A (304.25 ± 204.53 cells/mm2) than group B (953.44 ± 152.41 cells/mm2) and group C (758.91 ± 172.21 cells/mm2) (P<0.05). In group A, the body weight was gone down significantly comparison with other groups from fourth to seventh day after operation (P < 0.05).
This study demonstrates severe neuronal damage induced by CSD following global cerebral ischemia it can be postulated that this model may be one of the penumbra models to investigate pathology of cerebral ischemia and therapy.
|
